Among the different mechanisms mediating astrocyte toxicity towards neurons, functional impairment of the astrocyte plasmalemmal glutamate transporter EAAT2 has gained considerable interest as a potential therapeutic target from the milestone discovery that the antibiotic ceftriaxone enhances its expression and ameliorates the phenotype in mouse models of ALS [197] and FTLD-tau [156]. Here, MAPT is linked to amyotrophic lateral sclerosis.